Phorbol 12,13-Dibutyrate Increases Tyrosine Hydroxylase Activity in the Superior Cervical Ganglion of the Rat

Phorbol 12,13-dibutyrate (PDBu) increased the production of 3,4-dihydroxyphenylalanine (DOPA) in the superior cervical ganglion of the rat. This effect occurred without a detectable lag and persisted for at least 90 min of incubation. The action of PDBu was half-maximal at a concentration of approximately 0.1 microM; at high concentrations, PDBu produced about a twofold increase in DOPA accumulation. PDBu increased DOPA production in decentralized ganglia and in ganglia incubated in a Ca2+-free medium. The action of PDBu was additive with the actions of dimethylphenylpiperazinium, muscarine, and 8-Br-cyclic AMP, all of which also increase DOPA accumulation, and was not inhibited by the cholinergic antagonists hexamethonium (3 mM) and atropine (6 microM). Finally, PDBu did not increase the content of cyclic AMP in the ganglion. Thus, the action of PDBu does not appear to be mediated by the release of neurotransmitters from preganglionic nerve terminals, by the stimulation of cholinergic receptors in the ganglion, or by an increase in ganglionic cyclic AMP. PDBu also increased the incorporation of 32Pi into tyrosine hydroxylase. PDBu activates protein kinase C, which in turn may phosphorylate tyrosine hydroxylase and increase the rate of DOPA synthesis in the ganglion.     

Quantitative profiling of Arabidopsis polar glycerolipids in response to phosphorus starvation. Roles of phospholipases D zeta1 and D zeta2 in phosphatidylcholine hydrolysis and digalactosyldiacylglycerol accumulation in phosphorus-starved plants

Phosphorus is an essential macronutrient that often limits plant growth and development. Under phosphorus-limited conditions, plants undergo substantial alterations in membrane lipid composition to cope with phosphorus deficiency. To characterize the changes in lipid species and to identify enzymes involved in plant response to phosphorus starvation, 140 molecular species of polar glycerolipids were quantitatively profiled in rosettes and roots of wild-type Arabidopsis (Arabidopsis thaliana) and phospholipase D knockout mutants pld zeta1, pld zeta2, and pld zeta1 pld zeta2. In response to phosphorus starvation, the concentration of phospholipids was decreased and that of galactolipids was increased. Phospholipid lost in phosphorus-starved Arabidopsis rosettes was replaced by an equal amount of galactolipid. The concentration of phospholipid lost in roots was much greater than in rosettes. Disruption of both PLD zeta1 and PLD zeta2 function resulted in a smaller decrease in phosphatidylcholine and a smaller increase in digalactosyldiacylglycerol in phosphorus-starved roots. The results suggest that hydrolysis of phosphatidylcholine by PLD zetas during phosphorus starvation contributes to the supply of inorganic phosphorus for cell metabolism and diacylglycerol moieties for galactolipid synthesis.     

Different effects of phospholipase Dζ2 and non‐specific phospholipase C4 on lipid remodeling and root hair growth in Arabidopsis response to phosphate deficiency

Phosphate (Pi) deficiency in soils is a major limiting factor for plant growth. In response to Pi deprivation, one prominent metabolic adaptation in plants is the decrease in membrane phospholipids that consume approximately one‐third cellular Pi. The level of two phospholipid‐hydrolyzing enzymes, phospholipase Dζ2 (PLDζ2) and non‐specific phospholipase C4 (NPC4), is highly induced in Pi‐deprived Arabidopsis. To determine the role of PLDζ2 and NPC4 in plant growth under Pi limitation, Arabidopsis plants deficient in both PLDζ2 and NPC4 (npc4pldζ2) were generated and characterized. Lipid remodeling in leaves and roots was analyzed at three different durations of Pi deficiency. NPC4 affected lipid changes mainly in roots at an early stage of Pi deprivation, whereas PLDζ2 exhibited a more overt effect on lipid remodeling in leaves at a later stage of Pi deprivation. Pi deficiency‐induced galactolipid increase and phospholipid decrease were impeded in pldζ2 and npc4pldζ2 plants. In addition, seedlings of npc4pldζ2 had the same root hair density as pldζ2 but shorter root hair length than pldζ2 in response to Pi deficiency. The loss of NPC4 decreased root hair length but had no effect on root hair density. These data suggest that PLDζ2 and NPC4 mediate the Pi deprivation‐induced lipid remodeling in a tissue‐ and time‐specific manner. PLDζ2 and NPC4 have distinctively different roles in root hair growth and development in response to Pi deprivation; PLDζ2 negatively modulates root hair density and length, whereas NPC4 promotes root hair elongation.     

西南喀斯特石漠化生态系统土壤有机碳分布特征及其影响因素

喀斯特石漠化已成为制约我国西南地区社会经济可持续发展最严重的生态地质环境问题,其恢复重建已成为我国社会经济建设中一项重要内容。土壤有机碳作为土壤质量评价的重要指标,可以综合反映土地生产力、环境健康功能,另一方面土壤有机碳也间接影响了陆地生物碳库,是陆地生态系统碳平衡的主要因子,它的转化和积累变化直接影响全球碳循环动态,已成为生态科学领域研究的热点之一。系统的总结了西南喀斯特石漠化地区不同土地覆被/土地利用、不同等级石漠化环境土壤有机碳的空间和季节分布特征。结合前人研究成果,进一步分析了影响喀斯特石漠化地区土壤有机碳分布的自然(气候、地形与土壤性质、植被等)和人为(土地覆被/土地利用变化、农业管理措施等)各因素,并提出增加喀斯特石漠化地区土壤有机碳含量的对策。研究结果为喀斯特石漠化退化生态系统恢复重建、石漠化地区土壤综合利用、增加碳截存应对全球碳循环减源增汇等提供了重要的科学参考。     

Connections between sphingosine kinase and phospholipase D in the abscisic acid signaling pathway in Arabidopsis

Phosphatidic acid (PA) and phytosphingosine 1-phosphate (phyto-S1P) both are lipid messengers involved in plant response to abscisic acid (ABA). Our previous data indicate that PA binds to sphingosine kinase (SPHK) and increases its phyto-S1P-producing activity. To understand the cellular and physiological functions of the PA-SPHK interaction, we isolated Arabidopsis thaliana SPHK mutants sphk1-1 and sphk2-1 and characterized them, together with phospholipase Dα1 knock-out, pldα1, in plant response to ABA. Compared with wild-type (WT) plants, the SPHK mutants and pldα1 all displayed decreased sensitivity to ABA-promoted stomatal closure. Phyto-S1P promoted stomatal closure in sphk1-1 and sphk2-1, but not in pldα1, whereas PA promoted stomatal closure in sphk1-1, sphk2-1, and pldα1. The ABA activation of PLDα1 in leaves and protoplasts was attenuated in the SPHK mutants, and the ABA activation of SPHK was reduced in pldα1. In response to ABA, the accumulation of long-chain base phosphates was decreased in pldα1, whereas PA production was decreased in SPHK mutants, compared with WT. Collectively, these results indicate that SPHK and PLDα1 act together in ABA response and that SPHK and phyto-S1P act upstream of PLDα1 and PA in mediating the ABA response. PA is involved in the activation of SPHK, and activation of PLDα1 requires SPHK activity. The data suggest that SPHK/phyto-S1P and PLDα1A are co-dependent in amplification of response to ABA, mediating stomatal closure in Arabidopsis.     

Phospholipase D- and phosphatidic acid-mediated signaling in plants

The phospholipase D (PLD) family in higher plants is composed of multiple members, and each of the Arabidopsis PLDs characterized displays distinguishable properties in activity regulation and/or lipid preferences. The molecular and biochemical heterogeneities of the plant PLDs play important roles in the timing, location, and amount of phosphatidic acid (PA) produced. PLD-catalyzed production of PA has been shown to play important roles in plant growth, development, and response to various stresses, including drought, salinity, freezing, and nutrient deficiency. PLD and PA affect cellular processes through different modes of action, including direct target protein binding and biophysical effects on cell membranes. Improved knowledge on the mechanism by which specific PLDs and PA mediate given plant responses will facilitate the understanding of the molecular processes that connect the stimulus perception on membranes to intracellular actions and physiological responses.     

Arabidopsis sfd mutants affect plastidic lipid composition and suppress dwarfing, cell death, and the enhanced disease resistance phenotypes resulting from the deficiency of a fatty acid desaturase

A loss-of-function mutation in the Arabidopsis SSI2/FAB2 gene, which encodes a plastidic stearoyl-acyl-carrier protein desaturase, has pleiotropic effects. The ssi2 mutant plant is dwarf, spontaneously develops lesions containing dead cells, accumulates increased salicylic acid (SA) levels, and constitutively expresses SA-mediated, NPR1-dependent and -independent defense responses. In parallel, jasmonic acid-regulated signaling is compromised in the ssi2 mutant. In an effort to discern the involvement of lipids in the ssi2-conferred developmental and defense phenotypes, we identified suppressors of fatty acid (stearoyl) desaturase deficiency (sfd) mutants. The sfd1, sfd2, and sfd4 mutant alleles suppress the ssi2-conferred dwarfing and lesion development, the NPR1-independent expression of the PATHOGENESIS-RELATED1 (PR1) gene, and resistance to Pseudomonas syringae pv maculicola. The sfd1 and sfd4 mutant alleles also depress ssi2-conferred PR1 expression in NPR1-containing sfd1 ssi2 and sfd4 ssi2 plants. By contrast, the sfd2 ssi2 plant retains the ssi2-conferred high-level expression of PR1. In parallel with the loss of ssi2-conferred constitutive SA signaling, the ability of jasmonic acid to activate PDF1.2 expression is reinstated in the sfd1 ssi2 npr1 plant. sfd4 is a mutation in the FAD6 gene that encodes a plastidic omega6-desaturase that is involved in the synthesis of polyunsaturated fatty acid-containing lipids. Because the levels of plastid complex lipid species containing hexadecatrienoic acid are depressed in all of the sfd ssi2 npr1 plants, we propose that these lipids are involved in the manifestation of the ssi2-conferred phenotypes.